The objective of this work is to delineate the neuropsychologic factors which play a role in the genesis of cardiac arrhythmias. The specific focus continues on the patient with coronary heart disease who is susceptible to sudden death. The central hypothesis is that certain psychophysiologic mechanisms constitute transient risk factors which destabilize the ischemic myocardium and predispose to ventricular premature beats and ventricular fibrillation. Laboratory and clinical investigations will continue on: 1) neural influences on ventricular vulnerability; 2) changes in cardiac excitability during different stages of sleep in animals and man and 3) the influence of psychologic factors on ventricular vulnerability in normal animals and the occurrences of arrhythmias during myocardial ischemia. The work will extend to examining the effects of vagal stimulation on ventricular vulnerability in the conscious animal. Vagal ablation and stimulation will be conducted with and without sympathetic stimulation. The action of morphine and psychologic drugs on cardiac vulnerability will be evaluated. The effects of sleep on cardiac excitability will be pursued. The effect of mediation and other relaxation techniques on the prevalence of ventricular arrhythmias will be pursued. Examination of the role of psychologic stressors on the provocation of arrhythmias both in animals with coronary arterial occlusions and in patients with ischemic heart disease will be continued. BIBLIOGRAPHIC REFERENCES: Kolman, B.S., Verrier, R.L., and Lown, B. The effect of vagus nerve stimulation upon excitability of the canine ventricle: Role of sympathetic-parasympathetic interactions. Amer. J. Cardiol. (In press, 1976). Matta, R.J., Verrier, R.L., and Lown, B. The repetitive extrasystole as an index of vulnerability to ventricular fibrillation. Amer. J. Physiol. (In press, 1976).